ArticleGenetics2007
Reduced levels of Su(var)3-9 but not Su(var)2-5 (HP1) counteract the effects on chromatin structure and viability in loss-of-function mutants of the JIL-1 histone H3S10 kinase.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Drosophila P75 safeguards oogenesis by preventing H3K9me2 spreading.Journal of genetics and genomics = Yi chuan xue bao · 2020Article
- Set3 Is Required for Asexual Development, Aflatoxin Biosynthesis, and Fungal Virulence inFrontiers in microbiology · 2019Article
- H2Av facilitates H3S10 phosphorylation but is not required for heat shock-induced chromatin decondensation or transcriptional elongation.Development (Cambridge, England) · 2017Article
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- Genome-wide analysis of regulation of gene expression and H3K9me2 distribution by JIL-1 kinase mediated histone H3S10 phosphorylation in Drosophila.Nucleic acids research · 2014Article
- Histone H3 phosphorylation - a versatile chromatin modification for different occasions.Biochimie · 2012Review
- Enrichment of HP1a on Drosophila chromosome 4 genes creates an alternate chromatin structure critical for regulation in this heterochromatic domain.PLoS genetics · 2012Article
- The epigenetic H3S10 phosphorylation mark is required for counteracting heterochromatic spreading and gene silencing in Drosophila melanogaster.Journal of cell science · 2011Article
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- Global analysis of the relationship between JIL-1 kinase and transcription.PLoS genetics · 2011Article
- JIL-1 and Su(var)3-7 interact genetically and counteract each other's effect on position-effect variegation in Drosophila.Genetics · 2010Article
- Article
- Linker histone H1 is essential for Drosophila development, the establishment of pericentric heterochromatin, and a normal polytene chromosome structure.Genes & development · 2009Article
- RNA polymerase II-mediated transcription at active loci does not require histone H3S10 phosphorylation in Drosophila.Development (Cambridge, England) · 2008Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
It has recently been demonstrated that activity of the essential JIL-1 histone H3S10 kinase is a major regulator of chromatin structure and that it functions to maintain euchromatic domains while counteracting heterochromatization and gene silencing. In the absence of JIL-1 kinase activity, the major heterochromatin markers histone H3K9me2 and HP1 spread in tandem to ectopic locations on the chromosome arms. In this study, we show that the lethality as well as some of the chromosome morphology defects associated with the null JIL-1 phenotype to a large degree can be rescued by reducing the dose of the Su(var)3-9 gene. This effect was observed with three different alleles of Su(var)3-9, strongly suggesting it is specific to Su(var)3-9 and not to second site modifiers. This is in contrast to similar experiments performed with alleles of the Su(var)2-5 gene that codes for HP1 in Drosophila where no genetic interactions were detectable between JIL-1 and Su(var)2-5. Taken together, these findings indicate that while Su(var)3-9 histone methyltransferase activity is a major factor in the lethality and chromatin structure perturbations associated with loss of the JIL-1 histone H3S10 kinase, these effects are likely to be uncoupled from HP1.
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